表皮生长因子诱导人胰腺癌细胞SW1990中人宫颈癌基因的表达及其机制  

The Expression of Human Cervical Cancer Oncogene Induced by Epudernal Growth Factor in Pancreatic Cell SW1990 and Its Mechanism

作　　者：张盛[1] 蒋佳凯[1] 

机构地区：[1]常州市第三人民医院肝胆外科,江苏常州213000

出　　处：《苏州大学学报（医学版）》2011年第6期902-904,共3页Suzhou University Journal of Medical Science

基　　金：常州市社会发展科技计划项目(CS20102014)

摘　　要：目的研究表皮生长因子(EGF)诱导人胰腺癌细胞SW1990中人宫颈癌基因(HCCR)蛋白表达的分子信号通路机制。方法 100 ng/ml EGF作用SW1990细胞不同时间后,用Western blot检测其磷酸化AKT和HCCR蛋白表达情况;用LY294002(PI3K/AKT抑制剂)预处理SW1990细胞后用EGF作用SW1990细胞,观察其HCCR蛋白表达情况。结果 Western blot结果显示,与对照组相比,细胞内磷酸化AKT表达水平在4h时明显升高(P<0.05),而HCCR表达水平则随着EGF处理时间增加而升高(P<0.05);LY294002(PI3K/AKT抑制剂)可阻断EGF诱导的HCCR蛋白表达。结论 EGF通过PI3K/AKT通路诱导人胰腺癌细胞SW1990中HCCR蛋白的表达,这一通路可被PI3K/AKT抑制剂阻断。Objective To investigate the molecule mechanism of human cervical cancer oncogene （HCCR） expression induced by epidermal growth factor（EGF） in the pancreatic cells SW1990.Methods Treated with l00ng/ml EGF at different time,the expression of P-AKT and HCCR protein was detected by Western blot;Cells were pretreated with the specific inhibitor of PI3K/AKT（LY294002） and then cultured with EGF for 24h,the expression of HCCR protein in these cells were measured by Western blot.Results Western blot demonstrated that the expression of P-AKT reached the peak at 4h and then gradually decreased,but the expression of HCCR increased in a time-dependent manner.Treatment of the cells with PI3K inhibitor（LY294002） was able to significantly suppress HCCR expression induced by EGF.Conclusion EGF-induced HCCR over-expression in pancreatic cells SW1990 is mediated by PI3K/AKT signaling,which can be suppressed by its inhibitor.

关 键 词：表皮生长因子 SW1990细胞 人宫颈癌基因 

分 类 号：R735.9[医药卫生—肿瘤]